Maternal diet and obesity shape offspring central and peripheral inflammatory outcomes in juvenile non-human primates.
Chemokines
Cytokines
Maternal Obesity
Microglia
Neuroinflammation
Non-Human Primates
Nutrition
Western-Style Diet
Journal
Brain, behavior, and immunity
ISSN: 1090-2139
Titre abrégé: Brain Behav Immun
Pays: Netherlands
ID NLM: 8800478
Informations de publication
Date de publication:
05 2022
05 2022
Historique:
received:
22
10
2021
revised:
21
01
2022
accepted:
19
02
2022
pubmed:
27
2
2022
medline:
13
4
2022
entrez:
26
2
2022
Statut:
ppublish
Résumé
The obesity epidemic affects 40% of adults in the US, with approximately one-third of pregnant women classified as obese. Previous research suggests that children born to obese mothers are at increased risk for a number of health conditions. The mechanisms behind this increased risk are poorly understood. Increased exposure to in-utero inflammation induced by maternal obesity is proposed as an underlying mechanism for neurodevelopmental alterations in offspring. Utilizing a non-human primate model of maternal obesity, we hypothesized that maternal consumption of an obesogenic diet will predict offspring peripheral (e.g., cytokines and chemokines) and central (microglia number) inflammatory outcomes via the diet's effects on maternal adiposity and maternal inflammatory state during the third trimester. We used structural equation modeling to simultaneously examine the complex associations among maternal diet, metabolic state, adiposity, inflammation, and offspring central and peripheral inflammation. Four latent variables were created to capture maternal chemokines and pro-inflammatory cytokines, and offspring cytokine and chemokines. Model results showed that offspring microglia counts in the basolateral amygdala were associated with maternal diet (β = -0.622, p < 0.01), adiposity (β = 0.593, p < 0.01), and length of gestation (β = 0.164, p < 0.05) but not with maternal chemokines (β = 0.135, p = 0.528) or maternal pro-inflammatory cytokines (β = 0.083, p = 0.683). Additionally, we found that juvenile offspring peripheral cytokines (β = -0.389, p < 0.01) and chemokines (β = -0.298, p < 0.05) were associated with a maternal adiposity-induced decrease in maternal circulating chemokines during the third trimester (β = -0.426, p < 0.01). In summary, these data suggest that maternal diet and adiposity appear to directly predict offspring amygdala microglial counts while maternal adiposity influences offspring peripheral inflammatory outcomes via maternal inflammatory state.
Identifiants
pubmed: 35217175
pii: S0889-1591(22)00062-9
doi: 10.1016/j.bbi.2022.02.024
pmc: PMC8995380
mid: NIHMS1786628
pii:
doi:
Substances chimiques
Chemokines
0
Cytokines
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
224-236Subventions
Organisme : NIH HHS
ID : P51 OD011092
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH107508
Pays : United States
Organisme : NIMH NIH HHS
ID : K01 MH120507
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH124824
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH117177
Pays : United States
Informations de copyright
Copyright © 2022 Elsevier Inc. All rights reserved.
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